To show that Polycyclic Hydrocarbon Carcinogens produce mutations in areas of the genome of mammalian cells in culture which render the cells more liable to further genetic changes (a mutator type of mutation). To demonstrate that these mutations are important in initiating carcinogenesis by showing that clones with such mutations are, or quickly become,tumorigenic on hamster cheek pouch inoculation, whereas clones without such mutations are not tumorigenic. If successful, this will provide a tissue culture model of a modified somatic mutation theory of carcinogenesis. Polypeptide spectra and particular protein profiles of these clones will be studied to pick up any common changes in clones which achieve tumorigenicity. An increase in the variation of these in the clones which achieve tumorigenicity would support the presence of a mutator gene in these clones.